Induction of a glibenclamide-sensitive K-current by modification of a delayed rectifier channel in rat portal vein in insulinoma cells

In insulinoma cells (RINm5F), the glibenclamide-sensitive K-current (IK(ATP)) which developed spontaneously or after exposure to levcromakalim or to butanedione monoxime was always accompanied by a reduction in the delayed rectifier current (IK(V)). At potentials over which IK(V) was fully activated...

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Veröffentlicht in:British journal of pharmacology Jg. 110; H. 4; S. 1280
Hauptverfasser: Edwards, G, Weston, A H
Format: Journal Article
Sprache:Englisch
Veröffentlicht: England 01.12.1993
Schlagworte:
Animals
Benzopyrans - pharmacology
Cromakalim
Glyburide - pharmacology
Insulinoma - metabolism
Neurotoxins - pharmacology
Phosphorylation
Portal Vein - drug effects
Portal Vein - metabolism
Potassium Channels - drug effects
Potassium Channels - physiology
Pyrroles - pharmacology
Rats
Scorpion Venoms
Tumor Cells, Cultured
ISSN:0007-1188
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Zusammenfassung:In insulinoma cells (RINm5F), the glibenclamide-sensitive K-current (IK(ATP)) which developed spontaneously or after exposure to levcromakalim or to butanedione monoxime was always accompanied by a reduction in the delayed rectifier current (IK(V)). At potentials over which IK(V) was fully activated, the total outward current remained constant. In rat portal vein, the delayed rectifier channel inhibitor, margatoxin, reduced the combined induction of IK(ATP) and inhibition of IK(V) by levcromakalim. These data suggest that the ATP-sensitive K-channel, K(ATP), is a voltage-insensitive state of the delayed rectifier, KV.
Bibliographie:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
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ISSN:0007-1188
DOI:10.1111/j.1476-5381.1993.tb13955.x